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Article Released Sun-9th-August-2009 18:31 GMT
Contact: Ruth Institution: Nature Publishing Group
 Recovering movement after spinal cord injury in rats

Summaries of newsworthy papers include Instigator of type 1 diabetes?, p53 as a barrier to pluripotency, Inhibiting lymphatic vessel growth, How diverse is the microbial biosphere? and Mutations in rare human diseases


For papers that will be published online on 09 August 2009

This press release is copyrighted to the Nature journals mentioned below.

This press release contains:

· Summaries of newsworthy papers:

Neuroscience: Recovering movement after spinal cord injury in rats

Immunology: Instigator of type 1 diabetes?

Nature: p53 as a barrier to pluripotency

Medicine: Inhibiting lymphatic vessel growth

Methods: How diverse is the microbial biosphere?

And finally…Genetics: Mutations in rare human diseases

· Mention of papers to be published at the same time with the same embargo

· Geographical listing of authors

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[1] Neuroscience: Recovering movement after spinal cord injury in rats
DOI: 10.1038/nn.2377

Forepaw function in rats with severe spinal cord injury can be substantially improved through a combination of specialized exercises and treatment with specific proteins, reports a study online in this week’s Nature Neuroscience.

Presently, there is no treatment available to help quadriplegic patients regain function of their limbs after severe spinal cord injury. In animals, injection of an enzyme called chondroitinase into the spinal cord induces substantial growth of nerve fibers; however this undirected growth does not greatly improve limb function in the paralyzed animals.

James Fawcett and colleagues report that a course of therapy that combines training of fine forepaw function with chondroitinase treatment results in forepaw dexterity about twice that of rats who practiced without having received the chondroitinase injections.

Although possible side effects of chondroitinase injections into the spinal cord require much further study before such injections may be applied to human patients, these results suggest a possible new therapy for severe spinal cord injury.

Author contact:
James Fawcett (University of Cambridge, UK)
Tel: +44 122 333 1188; E-mail:

[2] Immunology: Instigator of type 1 diabetes?
DOI: 10.1038/ni.1773

Alterations in the activity of the Deaf1 protein may influence the onset of type 1 diabetes according to a study published online this week in Nature Immunology.

Diabetes is an autoimmune disorder induced by T cells that attack and destroy insulin-producing pancreatic beta-cells. Normally, T cells are made tolerant towards these pancreatic cells by exposure to self proteins.

C. Garrison Fathman and colleagues show that in mice Deaf1 facilitates the expression of these self proteins in pancreatic lymph nodes. However, they found that the expression of a non-functional form of Deaf1 coincides with the onset of type 1 diabetes.

Importantly, a similar non-functional form of Deaf1 is expressed in higher concentrations in type 1 diabetes patients than in healthy patients. Additional work is needed to determine if the loss of Deaf1 activity directly contributes to type 1diabetes onset, and if it is possible to therapeutically prevent expression of non-functional Deaf1 variants.

Author contact:
C. Garrison Fathman (Stanford University, CA, USA)
Tel: +1 650 723 7887; E-mail:

[3], [4], [5], [6] & [7] Nature: p53 as a barrier to pluripotency
DOI: 10.1038/nature08235
DOI: 10.1038/nature08311
DOI: 10.1038/nature08285
DOI: 10.1038/nature08287
DOI: 10.1038/nature08290

The well known molecule p53 serves not only as a tumour suppressor, but also acts as a barrier to the generation of induced pluripotent stem (iPS) cells. Five papers online in Nature this week show that when p53 is removed from cell populations that often fail to reprogram there is a higher degree of success.

The iPS cell field is fast moving — just three years ago stem cells were created from fibroblasts thanks to the insertion of four viral factors. Teams have tweaked the method, removing one or more of those factors. Shinya Yamanaka and colleagues managed to induce pluripotency in cells lacking p53 even without one of the four factors, and using a method that avoids genome integration of the factors. Juan Carlos Izpisua Belmonte and co-workers also demonstrate that reprogramming in the absence of oncogenes such as c-Myc and Klf4 occurs more efficiently when inactivating both p53 and another tumour suppressor. Another team led by Konrad Hochedlinger show that deletion of p53 in populations that do not reprogram rescues their ability to produce iPS cells, and that very high efficiencies can be achieved using immortalized cell lines that lack p53.

Maria Blasco and colleagues show that p53 is critically involved in preventing the reprogramming of cells carrying various types of DNA damage, including short telomeres. They go on to demonstrate that eliminating p53 allows efficient reprogramming even when there is DNA damage. Meanwhile Manuel Serrano and his team look at a tumour suppressor locus and report that the locus limits reprogramming. Furthermore, ageing has an effect on this locus, which means reprogramming is less efficient in cells from older organisms.

Authors contacts:
Shinya Yamanaka (Kyoto University, Japan) Author paper [3]
Tel: +81 71 751 3839; E-mail:

Juan Carlos Izpisúa Belmonte (The Salk Institute, La Jolla, CA, USA) Author paper [4]
Tel: +1 858 4534100, ext. 1130; E-mail:

Konrad Hochedlinger (Massachusetts General Hospital, Boston, MA, USA) Author paper [5]
Tel: +1 617 643 2075; E-mail:

Maria Blasco Spanish (National Cancer Research Centre, Madrid, Spain) Author paper [6]
Tel: +34 917 328 031; E-mail:

Manuel Serrano (Spanish National Cancer Research Center, Madrid, Spain) Author paper [7]
Tel: +34 917 328 000; E-mail:

[8] Medicine: Inhibiting lymphatic vessel growth
DOI: 10.1038/nm.2018

The discovery of the first endogenous inhibitor of lymphatic vessel growth is reported in this week’s Nature Medicine. The finding could potentially lead to treatment in cases of transplantation rejection and lymph vessel growth in tumours.

The lymphatic system is crucial in transporting fluids and molecules to cells as well as draining unwanted fluids. The disruption of the balance between positive and negative regulators for blood and lymphatic vessel growth can lead to many diseases, such as. Although many natural inhibitors of blood vessel growth exist, an endogenous selective inhibitor of lymphatic vessel growth – lymphangiogenesis – had previously not been described.

Jayakrishna Ambati and his colleagues report the existence of such an inhibitor, called soluble Vegfr-2. Soluble Vegfr-2 inhibits lymphangiogenesis by blocking signaling of the protein Vegf. In mice, tissue-specific loss of soluble Vegfr-2 induced spontaneous growth of lymphatic system to structures that normally lack lymphatic vessels, such as the cornea. Administration of soluble Vegfr-2 after injury or transplantation also inhibited lymphangiogenesis but not blood vessel growth, and therefore enhanced mice’s survival after graft surgery.

Owing to the selective effects of soluble Vegfr-2 on lymphatic vessels while sparing blood vessels, it might lead to potential treatments for lymphatic vascular malformations, transplantation rejection and tumor lymphangiogenesis.

Author contact:
Jayakrishna Ambati (University of Kentucky, Lexington, KT, USA)
Tel: +1 859 323 0686; E-mail:

[9] Methods: How diverse is the microbial biosphere?
DOI 10.1038/nmeth.1361

PyroNoise, an algorithm that accurately determines microbial diversity in an ecological sample from high-throughput pyrosequencing data, is presented online in this week’s Nature Methods.

During high-throughput pyrosequencing each base in a sequence is read as a flash of light and intensities of these light flashes are later converted to the four bases. It has been a valuable tool in assessing microbial diversity, but the challenge is to distinguish sequencing errors from true diversity. Sequences classified as comprising a new species may simply represent a known species with a few sequencing errors. This has led to an overestimation of microbial diversity and distorted phylogenetic trees constructed even when standard error correction methods – such as removal of ambiguous reads – were applied.

With PyroNoise, Christopher Quince and colleagues introduce an algorithmic solution for error correction. PyroNoise goes back to the primary data output – the light intensities that represent each base – and accurately calculates the correct sequence from these light intensities. This largely removes errors in the data and allows an accurate calculation of diversity within a sample.

Author contact:
Christopher Quince (University of Glasgow, UK)
Tel: +44 141 330 3556; E-mail:

[10] & [11] And finally…Genetics: Mutations in rare human diseases
DOI: 10.1038/ng.427

Mutations in the INPP5E gene lead to defects in the primary cilium – a microscopic antenna-like structure that protrudes from almost every cell in the mammalian body – according to two new studies published online in this week’s Nature Genetics. The studies report that defects in this structure lead to the genetic disorders MORM and Joubert syndrome.

Stephane Schurmans and colleagues found a mutation in INPP5E in individuals with MORM syndrome, a rare multi-organ disorder that is characterized by mental retardation, obesity, congenital retinal dystrophy and micropenis in males. Their experiments found that mutations in INPP5E led to decreased stabilization of the primary cilium, leading to multiple developmental defects.

In another study, Joseph Gleeson and colleagues discovered that other types of mutations in INPP5E lead to Joubert syndrome. This is a rare brain malformation that is characterized by the absence or underdevelopment of the cerebellar vermis, a brain region that controls balance and coordination. Common attributes of Joubert syndrome include abnormally rapid breathing, decreased muscle tone, atypical movements and mental retardation. The scientists found that the mutations in INPP5E lead to premature destabilization of primary cilia.

Authors contacts:
Stephane Schurmans (Universite Libre de Bruxelles, Gosselies, Belgium) Author paper [10]
Tel: +32 2 650 9825; E-mail:

Joseph Gleeson (University of California at San Diego, CA, USA) Author paper [11]
Tel: +1 858 822 3535; E-mail:

Items from other Nature journals to be published online at the same time and with the same embargo:

Nature (

[12] Topological surface states protected from backscattering by chiral spin texture
DOI: 10.1038/nature08308


[13] An essential role of the aPKC–Aurora A–NDEL1 pathway on neurite elongation by modulation of microtubule dynamics
DOI: 10.1038/ncb1919

[14] Organizer restriction through modulation of Bozozok stability by the E3 ubiquitin ligase Lnx-like
DOI: 10.1038/ncb1926


[15] Synthetic partial agonists reveal key steps in IP3 receptor activation
DOI: 10.1038/nchembio.195

[16] Cell-selective metabolic labeling of proteins


[17] Differentiation stage determines reprogramming potential of hematopoietic cells into iPS cells
DOI: 10.1038/ng.428

[18] FOXC1 is required for normal cerebellar development and is a major contributor to chromosome 6p25.3 Dandy-Walker malformation
DOI: 10.1038/ng.422


[19] Recruitment of the cytoplasmic adaptor Grb2 to surface IgG and IgE provides antigen receptor–intrinsic costimulation to class-switched B cells
DOI: 10.1038/ni.1764

[20] Coordination of multiple dual oxidase–regulatory pathways in responses to commensal and infectious microbes in drosophila gut
DOI: 10.1038/ni.1765

[21] TANK is a negative regulator of Toll-like receptor signaling and is critical for the prevention of autoimmune nephritis
DOI: 10.1038/ni.1771

[22] Tolerogenic signals delivered by dendritic cells to T cells through a galectin-1-driven immunoregulatory circuit involving interleukin 27 and interleukin 10
DOI: 10.1038/ni.1772


[23] Direct creation of three-dimensional photonic crystals by a top–down approach
DOI: 10.1038/nmat2507

[24] Mechanotransductive surfaces for reversible biocatalysis activation
DOI: 10.1038/nmat2504

[25] Surface-induced crystallization in supercooled tetrahedral liquids
DOI: 10.1038/nmat2508

[26] A dual-emissive-materials design concept enables tumour hypoxia imaging
DOI: 10.1038/nmat2509


[27] A granulocyte-macrophage colony–stimulating factor and interleukin-15 fusokine induces a regulatory B cell population with immune suppressive properties
DOI: 10.1038/nm.2003


[28] A customized and versatile high-density genotyping array for the mouse
DOI: 10.1038/nmeth.1359

[29] Digital transcriptome profiling using selective hexamer priming for cDNA synthesis
DOI: 10.1038/nmeth.1360

[30] BreakDancer: An algorithm for high resolution mapping of genomic structural variation
DOI: 10.1038/nmeth.1363


[31] Single europium-doped nanoparticles measure temporal pattern of reactive oxygen species production inside cells

[32] Monolayer coverage and channel length set the mobility in self-assembled monolayer field-effect transistors

[33] A quantitative fluorescence study of protein monolayer formation on colloidal nanoparticles


[34] High-sensitivity rod photoreceptor input to the blue-yellow color opponent pathway in macaque retina
DOI: 10.1038/nn.2353

[35] A face feature space in the macaque temporal lobe
DOI: 10.1038/nn.2363

[36] Cholinergic modulation of multivesicular release regulates striatal synaptic potency and integration
DOI: 10.1038/nn.2368

Nature PHYSICS (

[37] Direct observation ofmelting in a two-dimensional superconducting vortex lattice
DOI: 10.1038/nphys1368


[38] Insights into anaphase promoting complex TPR subdomain assembly from a CDC26–APC6 structure
DOI: 10.1038/nsmb.1645

[39] The molecular basis for the regulation of the cap-binding complex by the importins
DOI: 10.1038/nsmb.1649

[40] Existence of a microRNA pathway in anucleate platelets
DOI: 10.1038/nsmb.1651

[41] Cabin1 restrains p53 activity on chromatin
DOI: 10.1038/nsmb.1657


***The following paper will be published electronically on Nature Neuroscience’s website on 05 August at 2000 London time / 1500 US Eastern time. This paper is under embargo until this time, though the rest of the above articles on this release remain under embargo until 09 August at 1800 London time / 1300 US Eastern time ***

[42] SOX6 controls dorsal-ventral progenitor parcellation and interneuron diversity during neocortical development
DOI: 10.1038/10.1038/nn.2387


The following list of places refers to the whereabouts of authors on the papers numbered in this release. The listing may be for an author's main affiliation, or for a place where they are working temporarily. Please see the PDF of the paper for full details.

Buenos Aires: 22

Sydney: 18

Graz: 32

Minsk: 15

Brussels: 10
Gosselies: 10, 11
Liege: 10

Edmonton: 18
Montreal: 27, 40
Ottawa: 2
Quebec: 40

Cairo: 11

Palaiseau: 31
Paris: 31
Strasbourg: 24

Berlin: 17, 25
Braunschweig: 8
Bremen: 35
Goettingen: 8, 19
Hamburg: 17
Karlsruhe: 33
Mannheim: 5
Marburg: 33
Ulm: 33

Szeged: 11

Messina: 11
Pavia: 11
Rome: 11

Hyogo: 21
Ibaraki: 4
Kanagawa: 3, 13
Kawaguchi: 3
Kobe: 8, 13
Kyoto: 3, 4, 23
Osaka: 13, 21
Tokyo: 8, 13, 19
Yokohama: 8

Eindhoven: 32
Groningen: 32

Bergen: 9

Al-Khoud: 11

Moscow: 32

Kyungbuk: 20
Seoul: 20, 41
Suwon: 41

Barcelona: 4
Madrid: 6, 7, 37
Zaragoza: 37

Geneva: 42
Zurich: 11

Istanbul: 11

Al Ain: 11

Bath: 15
Cambridge: 1, 10, 15
Glasgow: 9
Liverpool: 9
Middlesbrough: 10
Newcastle: 9
Sheffield: 10
Uxbridge: 10


Berkeley: 34
Davis: 25
La Jolla: 4, 34
Pasadena: 16, 35
San Diego: 11
San Francisco: 3, 13
Santa Cruz: 34
Stanford: 2, 18

Gainesville: 2

Argonne: 38
Chicago: 18
Urbana: 33

Iowa City: 18

Lexington: 8

Shreveport: 8

Bar Harbor: 28

Bethesda: 14

Boston: 2, 5, 17, 35, 36, 42
Cambridge: 5, 17, 42
Charlestown: 35

St Louis: 10, 11, 30

New Jersey
Princeton: 12

New York
Ithaca: 39
New York: 35

North Carolina
Chapel Hill: 28
Durham: 26

Philadelphia: 18

Memphis: 38

Dallas: 8
Houston: 34

Salt Lake City: 8

Charlottesville: 26

Seattle: 29


For media inquiries relating to embargo policy for all the Nature Research Journals:

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Tel: +44 20 7843 4658; E-mail:

Neda Afsarmanesh (Nature New York)
Tel: +1 212 726 9231; E-mail:

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Tel: +44 20 7843 4562; E-mail:

For media inquiries relating to editorial content/policy for the Nature Research Journals, please contact the journals individually:

Nature Cell Biology (London)
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Nature Chemical Biology (Boston)
Andrea Garvey
Tel: +1 617 475 9241, E-mail:

Nature Genetics (New York)
Myles Axton
Tel: +1 212 726 9324; E-mail:

Nature Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; E-mail:

Nature Materials (London)
Vincent Dusastre
Tel: +44 20 7843 4531; E-mail:

Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail:

Nature Methods (New York)
Hugh Ash
Tel: +1 212 726 9627; E-mail:

Nature Nanotechnology (London)
Peter Rodgers
Tel: +44 20 7014 4019; Email:

Nature Neuroscience (New York)
Kalyani Narasimhan
Tel: +1 212 726 9319; E-mail:

Nature Photonics (Tokyo)
Oliver Graydon
Tel: +81 3 3267 8776; E-mail:

Nature Physics (London)
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Nature Structural & Molecular Biology (New York)
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